The problem with these studies is the mild symptom cases may never even be reported as cases, I know alot of people that had covid symptoms but never got tested, and would never get tested unless it got to the point where they needed medical care. So if you just had a "pretty bad" flu and sat at home you likely never got tested, and thus would never show up in these studies
Hell I know a couple people that were told by local medical center to not even bother with the test, they just assumed it was covid, was told to self isolate and monitor.
Both can be true - if you have a variant that is less deadly (but still deadly for some) and it is more transmissible then it will kill more people in absolute numbers. Also it can overwhelm hospitals, cuaing additional deaths and injuries (due to late treatment or treatment errors).
Delta is less deadly because more people have some immunity, either because of vaccination or because they have already been infected. Also it came late in the game, and many of the people who are the most at risk are already dead. Treatment has improved too.
So the virus itself isn't less deadly, it is just that we are better prepared.
the relative deadliness of delta... we'll just not ever really know. Though IIRC, some early surveillance with all the controls (only looking at unvaccinated, etc) suggested that it was LESS deadly for the elderly, more deadly for other age groups, net less deadly.
This is not necessarily the case for a virus with such a long period of asymptomatic transmission.
There is very little selective pressure for the virus to become less deadly; in fact, higher viron count is positively associated with both transmissibility and mortality.
Exactly. People overlook this fact constantly. There is no selection pressure for a virus like this to become more or less deadly. Just pressure to become more transmissible within our mixture of vaxxed, unvaxed, and some natural immunity.
I don't see how that negates my point. If the virus can mutate to have a longer transmissibility window, it implies that it will also be less deadly. The period when symptoms start is the period where your immune response is ramped up. Delaying or reducing the immune response implies longer transmission window and less severe illness.
Of course, if a virus killed you before you had a chance to pass it on then yes - but most viruses (including SARS-CoV-2) kill you slowly enough to have plenty of opportunity to propagate, there is no selection pressure to be less deadly.
To my knowledge, we have no evidence that any human virus has evolved to become less virulent (please furnish examples if I'm wrong!).
Unfortunately this common myth, that contagiousness is inversely correlated with lethality, has been used by those who would wish to downplay this public health disaster for whatever reason.
My understanding is that in fact we don't know. A likely explanation for its disappearance is that it ran out of susceptible hosts. Specifically, we have no evidence of a successor virus that was both less lethal, and induced immunity to the original.
I looked up Ebola to see if it has changed over time [0] and it looks like nada, since outbreaks are generally zoonotic, which means that the viral mutation-selection happens outside humans. Of note is Ebola's relation to Marburg, which was imported to Europe with Uganda-sourced lab monkeys.
Two large outbreaks that occurred simultaneously in Marburg and Frankfurt in Germany, and in Belgrade, Serbia, in 1967, led to the initial recognition of the disease. The outbreak was associated with laboratory work using African green monkeys (Cercopithecus aethiops) imported from Uganda. Subsequently, outbreaks and sporadic cases have been reported in Angola, the Democratic Republic of the Congo, Kenya, South Africa (in a person with recent travel history to Zimbabwe) and Uganda. In 2008, two independent cases were reported in travellers who had visited a cave inhabited by Rousettus bat colonies in Uganda. [1]
Replication-incompetent adenoviral vectors? Lex Fridman had a virologist on his podcast talking about the mutations done to the adenovirus to make it safe for the delivery of the s-protein (used in viral vector J&J + AstraZ vax). Maybe I misunderstood that?
For people, the difference between 2% and 0.2% mortality is huge, but for the virus (and the evolutionary pressures on it), the difference between 98% and 99.8% chance of continuing to spread is insignificant; any minor changes in the rate of spread far outweigh that. The evolutionary pressure towards survival of the host matter only for diseases with very high lethality.
Being more severe and deadly is not necessarily a propagation disadvantage.
Because if you sick you stay at home and don't go out. If you are very sick, you need to go to the doctor, or the hospital. This can create more spread.
wow, suddenly I feel like the film "Venom" was trying to teach me this, it's no good for the virus if it keeps killing its hosts, really its mutating itself while searching for a host that can coexist with it (as I understand it, much of our DNA is incorporated from viruses, but I don't understand it very well :)
It already coexisted with a host: bats. If we're going to anthropromorphize the virus, maybe it's searching for a way to kill off one of the biggest predators of its preferred host.
Let's go for endemy and be done with it. This vaccination chaos isn't more than trying to scoop water with a sieve. I'm 100% sure this is going to be one of the conclusions in 10 years. We are vainly shooting on a moving target with a musket from 100 meters. It's good effort and very lucrative but it won't work. Some people will die and some won't.
